HEART FAILURE

Definition
Heart failure is a complex clinical syndrome
that can result from any structural or functional
cardiac disorder that impairs the ability of the
ventricle to fill with or eject blood to meet the
metabolic demands of the body
 Heart Failure
This means less oxygen is reaching the organs and
muscles which can make feel tired and short of
breath.

CONGESTIVE HEART FAILURE refers to the state in

which abnormal circulatory congestion exists a
result of heart failure
 ETIOLOGY
systemic hypertension in 75% of cases.
Structural heart changes, such as valvular
dysfunction,cardiomyopathy,inflammatory heart
diseases
Arrythmias
Coronary Artery disease
Increase in Pulmonary pressure results fluid in alveoli
(PULMONARY EDEMA)
 Precipitating factors
Congenital heart defects
Severe lung disease
Diabetes
Severe anemia
Overactive thyroid gland (hyperthyroidism)
hypervolemia
Classification of heart failure
(1) According to the course of disease
1) Acute HF
2) Chronic HF

(2)According to the severity

1) mild HF or complete compensation
2) moderate HF or incomplete compensation
3) severe HF or decompensation
(4) According to the location of heart failure
1) Left -side heart failure (LHF)
2) Right-side heart failure (RHF)
3) Biventricular failure (whole heart failure)

(5)According to the function impaired

1) systolic failure
2) Diastolic failure
(3)According to the cardiac output (CO)
1) Low-output HF
2) High-output HF
 Pathophysiology

In order to maintain normal cardiac output,

several compensatory mechanisms play a
role to maintain normal tissue perfusion
including Compensatory enlargement in the
form of cardiac hypertrophy, cardiac
dilatation, or both.
 Compensatory Mechanisms
Sympathetic nervous system stimulation

Renin-angiotensin system activation

Ventricular hypertrophy

Ventricular dilatation
 Sympathetic Nervous System
Baroreceptors
o Nerve cells in carotid artery & aortic arch
o Maintain BP during normal activities
o React to increases & decreases in BP
decreased BP activates SNS; Release of
catacholamines, vasoconstriction of arterioles;
increases HR & heart contractility
RAAS MECHANISM
Renin-angiotensin system
Renin + Angiotensinogen

Angiotensin I

Angiotensin II

Aldosterone Secretion
Peripheral
Vasoconstriction
Salt & Water Retention

Inc.Plasma Volume Edema

Inc.Afterload
Inc. Preload
Cardiac Output
Inc.Cardiac Workload

Heart Failure
 VENTRICULAR DILATION
Dilation is an enlargement of the chambers of the heart
It occurs when pressure in the heart chambers is elevated
More stretching resulting increased cardiac output initially
 Hypertrophy
Hypertrophy is an increase in muscle mass and cardiac
wall thickness in response to overwork and strain
This will increase cardiac output initially
 Counterregulatory mechanisms
Body will try to maintain a balance in compensatory
mechanism
Heart muscles produce Natriuretic peptides
Atrial Natriuretic peptide(ANP)
b-type natriuretic peptide(BNP)
These are endothelin and aldosterone antagonists Which
will cause diuresis and vasodilation, prevent hypertrophy
Nitric oxide release vascular endothelium causes
vasodilation
 CLINICAL MANIFESTATIONS
1) Dyspnea
Exertional dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
2) Pulmonary edema
3) Fatigue
4) Tachycardia
5) edema
6) Behavioural changes
7) Skin changes
 CLINICAL MANIFESTATIONS
Right sided heart failure
Jugular venous distention
Hepatomegaly
Anasarca
Edema (pitting type)
Ascitis
weight gain
Tachycardia
Murmers
 CLINICAL MANIFESTATIONS
Left sided heart failure
pulmonary edema(crackles)
pleural effusion
s3 and s4 heart sounds
pulses alternans
changes in mental staus
displaced PMI, LV heaves
 COMPLICATIONS
Pleural effusion
Resulting from increased pressure in pulmonary capillaries
Dysrhythmias
Enlargement of chambers cause alterations in the normal
electrical pathway
Left Ventricular thrombus
enlarged LV and decreased CO combine to increase chance for
thrombus formation
Hepatomegaly
venous congestion causes hepatomegaly
Renal failure
 DIAGNOSIS
History: Risk factors for ischemic heart disease, family history
Physical exam: S3, JVD more specific signs of HF than rales,
peripheral edema
Chest X-ray - cardiomegaly and pulmonary edema; Kerleys B
Lines
Electrocardiogram- Anterior Q waves, LBBB, LVH
Echocardiogram- enlarged chambers, decreased ejection
fraction
Lab values- elevated ANP,BNP Levels
Hemodynamic- Reduced EF, Increased Pulm Cap Wedge
Pressure
Myocardial biopsy . Fulminant myocarditis
cardiac transplantation
 MANAGEMENT acute HF
GOALS
Decrease intravascular volume
Decrease venous return (preload)
Decrease Afterload
Improving gas exchange and oxygenation
Improving cardiac function
Reducing cardiac function
 Decreasing intravascular volume
Administration of diuretics
loop diuretics eg- Lasix(furosemide)
Ultrafiltration
Achieved by haemodialysis
 Decreasing venous return
It decreases the amount of volume returned to the
LV during diastole
Provide high fowlers position
Administration of IV nitroglycerine
 Decreasing afterload
Decreasing the systemic vascular resistance
IV sodium nitropusside
Morphine sulphate
Nesritide
recombinant form of BNP it causes both arterial and
venous dilation
 Improving gas exchange
Administration of oxygen by Oxygen mask or mechanical
ventilation
Administration of IV morphine sulphate
 Improving cardiac function
Digitalis- it is a positive inotrope that increases the force of
left ventricular contraction
Dopamine- beta adrenergic agonist, it will increases
contractility and heart rate
Dobutamine- synthetic beta adrenergic agonist, it does
not increase SVR
Milrinone and inamrinone- These are phosphodiestarase
inhibitors, they will enhances calcium entry ito cell and
increases contractility
 Reducing anxiety
Morphine sulphate
Benzodiazepines
Chronic heart failure
 CHF- Drug therapy
DIURETICS
Thiazide diuretics- first line drugs
Loop diuretics- commonly used
Spirinolactone- used as combination, blocks
the aldosterone effects on blood vessels
VASODILATORS
Eg- nitroglycerine, sodium nitropusside
 ACE inhibitors
first line therapy in treatment of CHF
eg- captopril and enalapril
Positive inotropes
digitalis glycosides
careful with side effects
beta adrenergic agonists
phosphodeesterase inhibitors
 Angiotensin receptor blockers ( ARB)
Used patient who are not tolerate ACE inhibitors
EG- losartan, telmisartan
Human beta natriuretic peptides
eg- Nesritide
Beta blockers
eg- atenelol, metoprolol
 Nutritional therapy
Diet education and weight management are critical to
the patient to control HF
Dietary restriction of sodium
mild HF- 2.5 gm salt
severe HF- 500-1000mg
Instruct to follow DASH diet
Fluid restriction
weigh regularly same time
weight gain of 1.4kg over 2 days inform health care
provider
 Non pharmacological
management
Intraaortic balloon pump(IABP)
Pacemaker therapy/Cardiac
resynchronization therapy(CRT)
Left ventricular assist device
Artificial heart
Heart transplantation
IABP
CRT PACEMAKER
VENTRICULAR ASSIST DEVICE
ARTIFICIAL HEART
 NURSING MANAGEMENT
Assessment
HEALTH HISTORY
PHYSICAL EXAMINATION
 Nursing diagnosis
Activity intolerance (or risk for activity intolerance) related to
imbalance between oxygen supply and demand because of
decreased CO

INTERVENTION
Barriers to performing an activity are identified, and methods
of adjusting an activity to ensure pacing but still accomplish the
task are discussed
Provide bedrest
The patients response to activities needs to be monitored
 Excess fluid volume related to excess fluid or sodium intake
or uncompromised regulatory mechanism
INTERVENTIONS
monitors the patients fluid status closely auscultating the lungs,
I/O chart , monitoring daily body weights, and assisting the patient to
adhere to a low-sodium diet
head of the bed may be elevated
assesses for skin breakdown and institutes preventive measures
Frequent changes of position, use of elastic compression stockings,
 Anxiety related to breathlessness and restlessness from inadequate
oxygenation
INTERVENTIONS
promote physical comfort and psychological support
involve family members to provides reassurance
speak in a slow, calm, and confident manner and maintain eye
contact
teaching ways to control anxiety and to avoid anxiety-provoking
situations